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LcpB regulates Staphylococcus aureus virulence and its interaction with host

ABSTRACT: Staphylococcus aureus is a significant Gram-positive human pathogenic bacterium that can give rise to skin and soft tissue infections and may also result in lethal diseases such as sepsis, pneumonia, endocarditis, osteomyelitis, etc. The cell wall of Staphylococcus aureus is a crucial immunogenic substance and participates in physiological processes like antibiotic resistance and virulence. The previous studies in the laboratory have indicated that the deletion of LCPB can upregulate the virulence of Staphylococcus aureus. However, the specific mechanisms by which LCPB regulates the virulence system of Staphylococcus aureus and its interaction with the host remain unclear. To explore the specific signal pathways by which lcpb regulates the interaction between Staphylococcus aureus and the host, we conducted proteomic experiments. This research discovered that both the knockout of LCPB and the application of WTA synthesis inhibitors can prevent the synthesis of the main component of the cell wall, wall teichoic acid (WTA), and upregulate the expression of excreted virulence factors such as HlgA, LukAB, and hla in Staphylococcus aureus. Subsequently, it was found that the central virulence regulation system agr of Staphylococcus aureus can respond to the reduction of WTA content, and the activation of agr is dependent on the expression of the two-component signal system saeRS.

ORGANISM(S): Mus Musculus

SUBMITTER: Baolin Sun

PROVIDER: PXD059233 | iProX | Wed Dec 25 00:00:00 GMT 2024

REPOSITORIES: iProX

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LcpB regulates Staphylococcus aureus virulence and its interaction with host

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